Disease relevance of Carcinoma in Situ

• The probability of being disease-free at five years survival among the patients with carcinoma in situ was 18 percent after treatment with doxorubicin and 45 percent after BCG therapy [1].
• The frequencies of other types of bladder carcinoma induced by N-butyl-N-(4-hydroxybutyl)nitrosamine were the following: mixed, 8%; squamous cell carcinoma, 42%; and carcinoma in situ, 3% [2].
• H-ras mutations were detected in 13 of 25 tissue specimens (10 of 14 invasive carcinomas and 2 of 4 carcinoma in situ, 1 of 5 dysplastic tissue, and 0 of 2 normal tissues) [3].
• COX-2 was not expressed in normal urinary bladder samples but was detected in 25 of 29 (86%) invasive transitional cell carcinomas of the urinary bladder and in 6 of 8 (75%) cases of carcinoma in situ [4].
• TCF17 mRNA levels are high in carcinoma in situ and in seminoma, a tumor derived from carcinoma in situ but still of low-grade malignancy [5].

High impact information on Carcinoma in Situ

• BRCA1 mRNA levels are markedly decreased during the transition from carcinoma in situ to invasive cancer [6].
• These results indicate a unique role for Egr1 in regulating the transition from localized, carcinoma in situ to invasive carcinoma [7].
• HPV16 VLP-specific IgGs were consistently detected in all women (n = 11) who were persistently HPV16 DNA positive during follow-up and whose disease ultimately progressed to CIN III (histologically diagnosed severe dysplasia or carcinoma in situ) [8].
• The incidence of carcinoma in situ for women in the study population (38.2 per 100,000) was 21% higher than that for White women (31.5 per 100,000) or for Black women (31.2 per 100,000) in the SEER population [9].
• These results confirm that the hyperbasophilic foci may be a population similar to carcinoma in situ or may be a direct precursor lesion of hepatocellular carcinoma [10].

Chemical compound and disease context of Carcinoma in Situ

• Effect of intravesical Bacillus Calmette-Guérin on detection of a urothelial differentiation antigen in exfoliated cells of carcinoma in situ of the human urinary bladder [11].
• The incidences of squamous cell carcinoma of the forestomach in MNNG-treated animals were significantly elevated by the diets containing CC (P less than 0.001), 2-tert-butyl-4-methylphenol (P less than 0.001), or p-tert-butylphenol (P less than 0.01), while the development of carcinoma in situ was inhibited by 4MP (P less than 0.01) [12].
• In blind analyses of cervical biopsies, obtained under direct vision by colposcopy of normal women (control) or from patients histopathologically diagnosed to have dysplasias or carcinoma in situ (study group), CRBP was not detectable by sucrose gradient analysis in 78.8% of the 33 abnormal biopsies, compared to 23.5% of the 34 controls [13].
• NHIK 3025 cells derived from a carcinoma in situ were exposed to hematoporphyrin derivative (Hpd) and light and examined by light microscopy, freeze-etching, scanning, and transmission electron microscopy [14].
• All lesions from any oral site that exhibited atypia diagnosed from hematoxylin and eosin stained sections as moderate-to-severe dysplasia or carcinoma in situ, whether hyperkeratotic or not, stained strongly for K19 in the basal and suprabasal cell layers [15].

Biological context of Carcinoma in Situ

• Allelic loss of p53 gene is associated with genesis and maintenance, but not invasion, of mouse carcinoma in situ of the bladder [16].
• Occurrence of chromosome 9 and p53 alterations in multifocal dysplasia and carcinoma in situ of human urinary bladder [17].
• Although low expression was present in testicular parenchyma with spermatogenesis, XIST was expressed at a higher level in parenchyma with carcinoma in situ, the precursor lesion of seminomas and nonseminomas [18].
• No cases of malignancy or carcinoma in situ were reported in the 121 cases of AIS where histology results were available [19].
• Methylation of RARbeta(50%), DAPK (75%), and E-cadherin (50%) was also detected in carcinoma in situ [20].

Anatomical context of Carcinoma in Situ

• Aberrant expression of MUC5AC and MUC6 gastric mucins and sialyl Tn antigen in intraepithelial neoplasms of the pancreas [21].
• In a subset of six patients whose most advanced lesion was carcinoma in situ without evidence of invasive cancer, p53 protein was detected in 0% of normal mucosas, 8.3% of squamous metaplasias, 37.5% of mild dysplasias, 12.5% of moderate dysplasias, 93.8% of severe dysplasias, and 55% of carcinoma in situ lesions [22].
• In contrast, a sharp demarcation is observed between E-cadherin-positive bladder cancer cells and the primary urothelium (carcinoma in situ pattern) [23].
• It has previously been reported that cytokeratin 19 (CK19), a 40-kd epithelial cytoskeletal protein within the suprabasal squamous epithelium, is a specific marker of moderate-to-severe dysplasia and carcinoma in situ in oral cavity squamous epithelium [24].
• Transcription factor AP-2gamma is a developmentally regulated marker of testicular carcinoma in situ and germ cell tumors [25].

Gene context of Carcinoma in Situ

• A low level of DAD-R expression is also observed in normal testicular parenchyma and in parenchyma containing the precursor cells of this cancer, i.e., carcinoma in situ [26].
• In contrast, a strong correlation between suprabasal expression of PCNA, a marker for proliferating cells, and dysplasia/carcinoma in situ was evident.(ABSTRACT TRUNCATED AT 400 WORDS)[24]
• Most carcinoma-in-situ lesions appeared to gain expression of cyclin D2 but not D1 or D3, while the invasive testicular tumours showed variable positivity for cyclins D2 and D3, but rarely D1 [27].
• Tumor infiltrating mononuclear cells from infiltrating carcinomas and carcinomas in situ expressed CD40 (10 of 10 cases), but less commonly CD40L (1 case of infiltrating lobular carcinoma, 2 cases of carcinoma in situ) [28].
• For SCC the sequence appears to include TP53 mutant clones in normal skin; dysplasia; carcinoma in situ; and SCC [29].

Analytical, diagnostic and therapeutic context of Carcinoma in Situ

• Both USC and its recently described putative precursor, endometrial intraepithelial carcinoma (EIC), demonstrate strong p53 overexpression by immunohistochemistry, suggesting alteration of the p53 gene in their pathogenesis [30].
• By microdissection, sequence analysis of the p53 gene, and analysis of loss of heterozygosity (LOH) at the site of this gene, we have now extended previous data to ascertain whether these p53 patches are precursors of simultaneously present squamous cell cancer or its morphologically recognized precancerous stages (dysplasia, carcinoma in situ) [31].
• We recently reported that noninvasive carcinoma in situ lesions of the human breast overexpress cyclin D, suggesting that this molecular event may represent a valuable target for chemoprevention [32].
• BACKGROUND: Intravesical instillations with bacillus Calmette-Guérin (BCG) is considered the treatment of choice in the prophylaxis of high-grade superficial bladder carcinoma and in the treatment of carcinoma in situ (CIS) of the bladder [33].
• Genomic DNA from 28 pancreatic IPMN tissue samples, categorized histologically as non-invasive intraductal IPMN (n = 3), IPMN with carcinoma in situ (n = 7), IPMN with microinvasion <1 mm (n = 4), and infiltrative IPMN with associated adenocarcinoma (n = 14), was modified by bisulfite treatment and analyzed with methylation-specific PCR (MSP) [34].

References